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Neuropsychological. Emotional. Personality and Pain Profiles in Litigating Whiplash Patients: Preliminary Evidence for Differentiation into Sub-Groups Based on Presence
and Level of Cervical Injury.
St. John's
by
Lorraine M. Dicks, M.Ps
A thesis submitted to the School of Graduate Studies
in partial fulfillment of the requirements for the degree of
Doctor of Philosophy
Department of Psychology Memorial University of Newfoundland
September 1998
Newfoundland
Abstract.
Neuropsychological, affective. personality. and physical consequences of post- concussion syndrome following an indirect blow to the head sustained through rapid acceleration/deceleration forces causing hyperextensionJbyperflexion (whiplash) injury were investigated. A mild traumatic brain injury comparison group (MTBI) was used.
All but one patient was involved in litigation at the time of their assessment. Whiplash patients were divided into three groups based on presence and level of cervical injury.
Patients with upper cervical spine injury were classified as the cervicoencephalic syndrome group (CES); lower cervical spine injury. the lower cervical spine syndrome (LCSS) group; and patients without structural damage. the ·no objective evidence of pathology· (NOEP) group. The study sought to substantiate this differential diagnosis.
Whiplash patients experienced fewer and less severe cognitive compromise than MTBI patients. In general. they were not memory impaired as was the MTBI group. The higher the level of neck injury. the greater the propensity for impaired anentional
functions and speed of information processing. This may be attributable to proximity of brainstem structures. Results provide preliminary support for the differentiation of whiplash patients into separate groups based on presence and level of cervical injury as proposed by Radanov eta/. (1992).
The NOEP group performed bener overall than any of the other groups on anentional measures and speed of information processing. This supports the belief that their injuries are less severe.
11
A predictable pattern emerged whereby as perceived pain intensity and interference due to physical discomfort increased. ability to control pain and activity levels decreased. and patients were more susceptible to depression. This pattern was most apparent in the CES group and tended in the same direction in the NOEP group. In
contrast. as perceived control of pain and activity levels increased. pain intensity and interference decreased. with less susceptibility to depression. This was most obvious in the head injured group and tended in the same direction in the LCSS group. Cognitive deficits following whiplash and MTBI were independent of levels of pain and coping responses to physical discomfort; emotional disturbance: and personality traits. That these patterns were not predictive of neuropsychological profiles suggests that they are based on different etiological origins.
iii
TABLE OF CONTENTS
Abstract . . . ii
List of Tables . . . x
List of Figures . . . xii
Acknowledgements ... ... ... ... .... .. ... . . xiii
Chapter I - INTRODUCTION ... .. ... .. ... ... ... .... ... . ... 1
1.1 Post Concussion Syndrome Fallowing Mild Traumatic Brain Injury ... . 1
1.1.1 Definitions ... ... .. . .. .. ... ... .. . .. . 1
1.2 Cerebral Symptoms Caused by Hyperextension!Hyperflexion Injury to the Neck . . . ... ... ... ... .. ... ... 4
1.3 Incidence and Economic Impact .... ... ... .. 7
1.4 Post Concussion Symptoms .. ... ... ... .. .... .. ... . ... II 1.4.1 Physical Sequelae .... ... ... .. .... .. ... .. .. II 1.4.2 Cognitive Sequelae .. ... . ... . ... . . 16
1.4.3 Emotional Sequelae .. ... ... ... ... .. ... . 18
1.4.4 Symptom Interaction ... ... ... ... ... .. . 30
1.5 Pathogenesis of Post Concussion Symptoms: ... ... . ... 33
1.5 .1 Neuropsychological Mechanism of Action ... 3 3 1.5 .2 The Kindling Model. . . . 3 8 1.6 Purpose of the Study ... ... ... . .... 40
iv
1.7 Research Objectives ... 42
1.7.1 Hypothesis 1. ... 43
1. 7.2 Hypothesis II ... 43
1.7.3 Hypothesis III. ... ... .. ... 43
1 . 7.4 Hypothesis IV. . ... ... .. 44
Chapter II • METHODS ... 45
2.1 Subjects ... ... 45
2.2 Procedures ... 48
2.3 Neuropsychological Assessment. ... 49
2.3.1 Wechsler Adult Intelligence Scale·Revised (WAIS·R) ... 50
2.3.2 Wechsler Memory Scale-Revised (WMS-R) ... ... 52
2.3.3 Wisconsin Card Sorting Test (WCST) ... ... . 52
2.3.4 Verbal Fluency (FAS) ... ... ... ... 53
2.3.5 Complex Anentional Functions ... 53
2.3.5.1 Paced Auditory Serial Addition Test (PASAT). . ... 54
2.3.5.2 Bro~n-Peterson Consonant Trigrams (CCC) ... 54
2.3.5.3 Trail Making Test (TMT) ... ... 55
2.4 Personality Assessment ... 56
2.4.1 Millon Clinical Multiaxial Inventory (MCMI). . ... 56
2.4.2 Beck Depression Inventory (BDI) ... 57
2.4.3 Spielberger State-Trait Anxiety Inventory (ST AI). . ... 58 v
2.5 Assessment of Pain ... ... ... 58
2.5.1 West Haven Yale Multidimensional Pain Inventory (WHYMPI). 58 2.6 Statistical Analyses ... ... .... 59
2.7 Use ofNonnative Data ... . 60
Chapter III - RESULTS ... 62
3.1 Demographics. . ... 62
3.2 Neuropsychological Findings ... ... 62
3.2.1 Wechsler Adult Intelligence Scale-Revised (WAIS-R) .... ... . 64
3.2.2 Wechsler Memory Scale-Revised (WMS-R) Comparisons between General Memory Quotient (GMQ). Delayed Memory Quotient (DMQ) and Attention-Concentration Quotient (Attn Q) to Nann. . ... 67
3.2.3 Brown-Peterson Consonant Trigrams (CCC) ... ... 69
3.2.3.1 9-Second Delay Recall Trial. ... ... ... 69
3 .2.3 .2 18-Second Delay Recall Trial. ... 72
3.2.4 Trail Making Test (TMT) ... .. ... ... 75
3.2.4.1 Part A. . ... 75
3.2.4.2 Part B ... 77
3.2.5 Paced Auditory Serial Addition Test (PASAT). . ... 79
3 .2.5 .1 All Pacing Intervals ... 80
vi
3 .2.6 T-Tests Comparing Means on Each Trial of the P ASA T to
Nonnative Values in Each Patient Group ... 80
3.2.6.1 3.2.6.2 3.2.6.3 2.4 Second Interval. . ... 82
2.0 Second Interval ... 82
1.6 Second Interval. . ... 82
3.2.7 Verbal Fluency Test (FAS) ... 82
3.2.8 Wisconsin Card Sorting Test (WCST) ... 85
3.2.8.1 Categories Generated. . ... 85
3.2.8.2 Perseverative Errors. . ... 85
3.3 Personality I Emotional Assessment ... 85
3.3.1 Millon Clinical Multiaxiallnventory (MCMI) ... 85
3.3.2 Beck Depression Inventory (801) ... ... 87
3.3.3 Spielberger State-Trait Anxiety Inventory (STAI) ... 89
3.3.3.1 3.3.3.2 State Anxiety. . ... 89
Trait Anxiety ... 89
3.4 Pain Assessment ... ... 90
3.4.1 West Haven Yale Multidimensional Pain Inventory (WHYMPI) ... 90
3.4.2 Pain Severity ... 91
3 .4.3 Interference. . ... 91
3.4.4. Pain Control. ... 91 vii
3.4.5 General Activity Level. ... ... ... 93
3.5 Relationship of Neuropsychological Variables to Pain Depression and Anxiety ... .. .. .... ... .. .... 93
Chapter IV - DISCUSSION . . . 98
4.1 Demographics ... 98
4.1.1 Gender ... 98
4.1.2 Age ... ... ... ... ... .. ... 99
4.2 Interpretation ofNeuropsycho1ogical Test Results .... .. ... ... . 99
4.2.1 lntelligence ... .... .. .... ... 100
4.2.2 Memory ... ... .. ... .. 103
4.2.3 Mild Traumatic Brain Injury ... 104
4.2.4 LCSS ... .. ... .. ... 1 04 4.2.5 NOEP ... 105
4.2.6 CES ... .. ... ... 105
4.3 Summary of Memory Results. . ... 106
4.4 Attention/Concentration ... ... ... 1 07 4.5 Brown-Peterson Consonant Trigrams (CCC). . ... 110
4.6 Information Processing Speed ... 113
4.6.1 Trail Making Test (TMn ... 113
4.6.2 Paced Auditory Serial Addition Test (PASAn ... 114
4.6.3 Verbal Fluency (FASTest) ... 118 viii
4. 7 Executive Functions ... 119
4. 7.1 Wisconsin Card Sorting Test (WCST). . ... 119
4.8 Personality and Affective Symptoms ... 120
4.8.1 Depression and Anxiety ... 123
4.9 Pain ... .. ... ... .... 126
4.10 Relationship of Neuropsychological Variables to Depression Anxiety and Pain . . . 128
4.11 Medication Effects ... ... ... .... ... . .. ... ... . 132
4.12 Litigation Considerations .. .... ... ... . 133
5.0 Summary . . . ... .... ... ... ... .. .. .. 136
5.1 Directions For Future Research ... 139
References ... 142
Appendix A ... 168
Appendix 8 . . . 166 Appendix C ... 1 70 Appendix D . . . 1 71
ix
LIST OF TABLES
Table 1. Patient Demographics .... ... ... ... .... ... ... 63 Table 2. T-Tests Comparing Full Scale IQ (FSIQ) per Group to Normative Mean .... . 66 Table 3. T-Tests Comparing General Memory Quotient (GMQ) per Group to Normative
Mean ... ... .... .... ... ... ... .... ... .. ... ... 68 Table 4. T-Tests Comparing Delayed Memory Quotient (DMQ) per Group to Normative
Means ... ... ... .... ... .. .. .. ... .. ... 70 Table 5 . T-Tests Comparing Attention/Concentration Quotient (Att/Con) per Group to
Normative Means . ... .... ... ... .... .. ... .... ... .. .. .... 71 Table 6a. Consonant Trigrams. T-Tests Comparing Sample Means to Mean
ofNormative Population for Number of Consonants Recalled Out of Fifteen After a 9 Second Interpolated Task .. ... ... ... ... ... 73 Table 6b. Consonant Trigrams. T-Tests Comparing Sample Means to Mean
of Normative Population for Number of Consonants Recalled Out of Fifteen After an 18 Second Interpolated Task .. ... ... ... 73 Table 7a. Trail Making Test Part A. T-Tests Comparing Group Means to Normative
Mean for Time to Task Completion ... ... ... .... ... 78 Table 7b. Trail Making Test Part B. T-Tests Comparing Group Means to Normative
Mean for Time to Task Completion. . ... ... .... 78
X
Table 8. Percentages in each group who were able to complete the P ASA T. . ... 81 Table 9a. Paced Auditory Serial Addition Test. T-Tests Comparing Group Mean to
Normative Mean on the 2.4 Second Pacing of the P ASA T. . ... 83 Table 9b. Paced Auditory Serial Addition Test. T-Tests Comparing Sample Variance to
Normative Mean on the 2.0 Second Pacing of the PASAT . ... ... .... 83 Table 9c. Paced Auditory Serial Addition Test. T-Tests Comparing Group Mean to
Normative Mean on the 1.6 Second Pacing of the P ASA T. ... .... 83 Table 10. Results of Multiple Regression Analysis of Pain Severity (WHYMPI). State
and Trait Anxiety (STAI) and Depression (BDI) on Delayed Recall (\VMS-R)
(N =44) ... .... .... ......... .... .... 95
Table 11. Results of Multiple Regression Analysis of Pain Severity (WHYMPI). State and Trait Anxiety (STAI) and Depression (801) on Attention Concentration (WMS-R) (N =46) .... .. ... . ... .. . . 96 Table 12. Results of Multiple Regression Analysis of Pain Severity (WHYMPI). State
and Trait Anxiety (ST AI) and Depression (BDI) on the P ASA T 2.4 (N ==46). . . 97
xi
List of Figures
Figure 1. Comparisons between nonnative and average FSIQ with the GMQ.
DMQ and ATT/CON Q ofthe WMS·R .. .... .. ... ... ... .. 65 Figure 2. Comparisons of group means to normative means on the Consonant
Trigram Test (CCC) ... ... .. ... ... ... .... 74 Figure 3. Comparisons of group means to normative means on the Trail Making
Test (TMT) .... ... .... ... .... ... ... ... ... ... ... 76 Figure 4. Comparisons of means of groups to normative means on the Paced
Auditory Serail Addition Test (P ASA T) ... ... ... ... ... ... . 84 Figure 5. Millon Clinical Multiaxiallnventory (MCMI) ... .... ... ... ... .. 86 Figure 6 . Plots of pain. anxiety and depression ... ... .. .. ... .... ... ... 88 Figure 7. Pain measures by injury group .... ... ... ... ... ... .. ... ... .. 92
xii
Acknowledgments
I would like to thank my supervisor. Dr. Robert Adamec who provided his expertise and time in guiding me throughout the process of completing all aspects of my doctoral program over the past several years. I would also like to express my
appreciation to Dr. Francine Sarazin who served on my committee and ensured that all neuropsychological aspects of my study were sound. A special thank you is also extended to Dr. Mark Howe whose expertise in cognitive psychology and statistics was also
appreciated and contributed to the quality of this work.
I would like to acknowledge the support of the late Dr. A. E. Shapter. Orthopaedic Surgeon. who worked tirelessly with this patient population to ensure they received the medical respect they deserved despite the complexity of their symptoms. Through consultations on clinical cases. Dr. Shapter contributed to the evolution of my thoughts on these patients which allowed me to refine my original hypothesis.
During the years I worked in Ottawa. I valued the clinical supervision provided to me by the late Dr. Clare Stoddart. She contributed to my knowledge of both
neuropsychological assessment procedures as well as interpretation of test results. I also gratefully acknowledge her editorial comments in contributing to my current writing style.
Dr. Abraham Ross was always available throughout my program and served as ··a port in the storm'" whenever I felt I needed advise.
Without the support of my husband. Dr. Benjamin Davis. I would likely never have found the time or patience to persevere with my studies to completion. His knowledge in use of computer software was also invaluable. Our daughters. Katie.
Madeline. and Claire were very patient over the years when Mommy was doing her homework.
xiii
INTRODUCTION
1.1 Post Concussion Syndrome Following Mild Traumatic Brain Injury
Post-concussion syndrome (PCS) typically refers to a constellation of symptoms following a direct blow to the head (Szmanski and Linn. 1992). Studies on the physical effects of intracranial brain movement have also demonstrated that PCS can occur in individuals subjected to extreme acceleration forces in motor vehicle accidents (MY A· s) without direct impact to the head and in the absence of loss of consciousness (LOC) (Batjer. Cole Kopitnik and Purdy, 1992: Sweeney 1992). Taylor. Cox and Mailis ( 1996) suggest that whiplash can represent one of the mildest forms of head injury. Sweeney (1992) also assens that victims of non-impact acceleration forces often meet diagnostic criteria for mild head injury. Although this suggests that the symptoms have a primarily organic etiology, it has been argued that the syndrome also has psychological origins (Mariadas. Chitra, Gangadhar and Hegde 1989; Putnam, Millis and Adams 1996).
1.1.1 Definitions
Several classification schemes have been designed to determine head injury severity based on initial and changing neurological findings over time. Although these criteria vary to some degree, salient classification features include: a transient loss or alteration of consciousness following trauma to the head with resultant post-traumatic amnesia (PTA) which does not exceed 20 minutes around the injury event; Glasgow Coma Scale score (GCS) of 13 to 15; and hospitalization ofless than 48 hours (Davidoff, Kessler. Laibstain and Mark 1988; Putnam et al. 1996). The American Congress of Rehabilitation Medicine confers the term "mild traumatic brain injury" on patients who
2 report feeling dazed or stunned follo\\ling an accident and includes a whiplash injury, even when GCS ratings are perfect and no obvious loss of consciousness (LOC) has occurred (Taylor eta/. 1996). It has been estimated that up to 50% of patients who suffer mild head injuries experience cognitive disturbances in a few days to weeks following the initial insult (Joseph 1990). These cognitive effects usually return to normal
approximately three months post-injury (Stuss. Ely. Hugenholtz. Richard. LaRochelle.
Poirier and Bell 1985). Although variable in degree and duration. post-concussion symptoms may persist in a subgroup of patients for extended periods of months to years after the event (Levin, Eisenberg and Benton 1991; Yarnell and Rossie 1988). This is long after the expected recovery time (Binder 1986; Taylor era/. 1996).
There are three major types of post-concussional symptoms associated with mild head injury that evolve in the initial hours following trauma (Anderson 1995). The first symptom group includes physical complaints such as headache. fatigue, insomnia.
dizziness. hyperacusis, photophobia and alcohol intolerance. The second group of symptoms involve affective or emotional changes characterized by increased irritability and low frustration tolerance, anger and generalized anxiety. Dysphoria or depression, as well as aspontaneity and reduced initiative are also common. Finally, sufferers of mild head injury complain of persistent cognitive sequelae. These include impaired attention and concentration, memory problems, slowed reaction time, and diminished rate of information processing, as well as mental inertia.
3 Cognitive and neurobehavioral sequelae of the post-concussive syndrome (PCS) following mild head injury persists in a subgroup of patients beyond time limitations anticipated based on the original severity of impact (Hugenholtz. Stuss. Stethem and Richard 1988). Although the contention that persisting sequelae which occur after mild head injury are insupportable. the possibility of selective vulnerability of some patients should be considered to differentiate those who are at risk for long-term consequences from those who are not. The level of disruption in patients who experience persistent complaints can lead to vocational disability (Blankenship 1988: Hurt 1991 ): interpersonal discord (Bohnen and Jolles 1992): as well as to psychopathology including anxiety and depression. Whether these symptoms are of primarily physiogenic or psychogenic etiology continues to be debated (Bohnen and Jolle~ 1992~ Putnam eta/. 1996). This controversy is partially fuelled by the dis-proportionality of symptoms to the original insult as well as to the absence of identifiable central nervous system lesions on standard neuro-imaging techniques (Schwartz. Barth. Dane. Drenan. DeGood and Rowlingson 1987; Anderson 1995). The presence of confounding effects such as litigation in many of the afflicted patients has led to the diagnosis of malingering, compensation neurosis. or secondary gain (Mckinlay, Brooks and Bond 1983; Schwartz eta/. 1987; Youngjohn et a/. 1995).
Until recently people who sustained mild head injury remained largely neglected by the medical profession except for the provision of acute treatment with discharge from the emergency room. Although they now receive increased assessment, almost no
emphasis is placed on follow-up intervention either medically or psychologically until their condition has become more chronic (Bohnen and Jolles 1992).
4
1.2 Cerebral Symptoms Caused by Hyperextension!Hyperflexion Injury to the Neck.
Hyperextensionlhyperflexion injury to the neck, commonly referred to as a whiplash injury. can be sufficient to cause cerebral symptoms similar to those follO\\ing mild head injury. This can occur in the absence of an apparent direct physical impact to the head (Yarnell and Rossie 1988~ Sweeney 1992). These types of injuries are
particularly numerous in patients who experience rapid acceleration/deceleration forces to the neck through a whiplash mechanism such as that encountered in motor vehicle
accidents {Chapman-Smith 1988). The presence of minor brain trauma. sustained through a whiplash mechanism. has been postulated based on the similarity of symptoms
following whiplash with those of Post Concussive Syndrome (PCS) following mild traumatic brain injury (Teasell eta/. 1993 ). While there is some credible evidence of an organic etiology for post-traumatic symptoms following concussion. its presence after uncomplicated whiplash remains more questionable due to lack of evidence (Tease II eta/.
1993; Radonov eta/. 1993).
Pioneer work on neurophysiological change following concussion demonstrated
pennanen~ traumatically-generated damage characterised by microscopic capillary hemorrhages and neural lesions as well as reduced cerebral blood flow (Oppenheimer 1968). This early work is often cited to support the view that concussion falls on a continuum and represents a mild form of diffuse brain injury. Oppenheimer (1968)
5
further proposed that these neurophysiological changes reflect disruption to bilateral anterior and cortical-subcortical connections. Although the prognosis of whiplash patients is variable, it has been estimated that symptoms persist for at least six months in more than a quarter of affiicted patients (Spitzer. Skovron, Salmi. Cassidy, Duranceau, Suissa
1995).
Rapid acceleration forces to the head causes brain tissue to accelerate at a different rate than bone due to differential densities between the two. Differences also exist between white (pathways) and gray (cell bodies) matter regions. This creates a gradient that results in shearing forces on brain tissue (Bigler 1990). Ommaya and Gennarelli ( 197 4) proposed that the whiplash mechanism involves inertial impulse
loading that results in localized involvement of limbic and fronto-orbito-temporal cortices as well as in the brainstem and upper cervical spinal cord (Sweeney 1992). These regions demonstrated increased susceptibility to damage due to maximal centripetal. structural and tissue density (Binder 1986). The strain involved following such acceleration- deceleration forces cause not only a shearing of a.xons but a resultant degeneration over time of neural tracts in the brainstem (Joseph 1990). The effects of the shear/strain mechanism begin at the surface of the brain in mild cases and extend inward to involve the diencephalic - mesencephalic core following more severe trauma (Ommaya and Gennarelli 1974). It has been suggested that concussion symptoms likely result from
"structural or electrical interference with ascending reticular pathways" (Mesulam 1985).
Extreme or rapid extension of the head may cause decreased blood flow to the brain by compressing the vertebral arteries which supply the brainstem. cerebellum.
occipital lobe and hippocampal region of the temporal lobe (Joseph 1990). The internal carotid artery exposed in the neck is also vulnerable to injury under conditions of rapid extension or rotation that can contribute to further trauma. Although speculative. it has been postulated that the cause and effect of cerebral ischemia after trauma creates neuronal abnormalities in the cranial-spinal junction that leads to altered cerebral blood flow (Joseph 1990). Prolongation of vasoconstriction and vasomotor dysregulation has been hypothesised as another of the possible mechanisms which might contribute to the persistence of PCS (Binder 1986).
6
In an investigation of electroencephalograms (EEG) of post-whiplashed monkeys.
King Liu. Chandran. Heath and Unterharnscheidt ( 1984) found electrophysiological disturbances in the brain particularly in the hippocampal region. They considered the growth and development of this trauma-induced hippocampal spiking to be a subclinical form of post-traumatic epilepsy (King Liu eta/. 1984 ). When subcortical EEG changes did take place, normal or mild abnormal tracings were obtained from scalp EEGs. When the whiplashed animals developed abnormalities, they occurred at least six weeks post- whiplash.
Since then cognitive deficits involving attentional functions were demonstrated in whiplashed patients even without a speculated mild traumatic brain injury (Radonov eta/.
1992). These deficits were considered secondary to headache caused by cervical
7
pathology. Schwartz et al. ( 1987) however, caution against the misattribution of cognitive problems to pain. In a prospective study. Radonov eta/. (1993) found a direct relationship with ongoing symptomatology following whiplash with factors linked to trauma, age.
presence of previous head injury and, in particular, reduced cognitive acuity as a result of the injury. Psychosocial factors. personality traits and negative affect were not
determinants of the development or duration of symptoms following cervical strain.
1.3 Incidence and Economic Impact
A cohort study conducted by a Quebec task force was struck to investigate various aspects of whiplash associated disorders (WAD). The source population for this
epidemiological study was comprised of all people who suffered a whiplash injury in a MV A in 1987 in Quebec and who submitted a claim through the provincial insurance service. The study found the population-based annual incidence rate of compensated insurance claims for whiplash injury was 70 per 100,00 inhabitants. This resulted in more than 18 million dollars paid out to 4757 patients. Over 70% of this money accounted for payment for replacement of lost regular income. The study revealed that the incidence of claims was notably higher in females than males across different age groups. It was speculated that this was attributable to the fact that given the same head size, men have more neck musculature than women, making them less prone to suffering whiplash injury ( 1995). It was also proposed that women may be more inclined to seek compensation than men. In addition, regional variation in incidence of claims existed which appeared to be correlated with population density and the number of commuters in each region.
8 Although research is limited. and time estimates for recovery are variable. it is established that post-concussion symptoms following either a direct or indirect blow to the head such as a whiplash injury can linger in a subgroup of patients for long periods.
Symptoms can last from months to years or even indefinitely. The economic toll of these residual problems can delay or prohibit resumption of work. wreak havoc in personal lives. generate stress reactions and contribute to ongoing discomfort. This situation is critical given that approximately fifty percent of people who suffer mild traumatic brain injury are at risk of developing post-concussive symptoms (Joseph 1990). Eighty-one percent of head injuries are classified as mild. This translates into an incidence rate of 131 per 100.000 individuals or 35.000 Canadians per year. The nonspecific nature of those symptoms associated with mild traumatic brain injury make them difficult to quantify or to document objectively.
Compared to other trauma-related injuries. soft tissue injury of the cervical spine is disproportionately associated with litigation. Whiplash injury is common among motor vehicle occupants following collision. The incidence rate varies greatly in different parts of the world with the annual estimated rate as high as l 06 per 1 00,000 in Australia (Spitzer eta/. 1995). Bannister and Gargan (1993) state that 56% of cases presenting to the Accident Board in Victoria Australia over a six month period who suffered such injury are involved in litigation. In Quebec, whiplash represents the most common type of injury for which claims have been filed with the local insurance service. In British
Columbia and Saskatchewan, both provinces with single payer motor vehicle insurance
programs ("No-fault"), 68% and 85% of their respective claims are paid to whiplash patients (Spitzer eta/. 1995). This represents a substantial financial burden for the insurance system.
Approximately 6.5 million motor vehicle accidents occurred in the United States in 1994. of which 3.2 million resulted in injuries. Eighteen percent of these accidents involved rear-end collisions that caused injury to an estimated 500.000 people. These rear-end impacts result in a higher incidence of whiplash associated disorders than any other type of injury (Brault. Wheeler. Siegmund and Brault 1998).
9
Taylor eta/. ( 1996) projected an annual hospitalization cost for Americans in excess of$1 billion following whiplash injury. A similar extrapolation from 1981
projected a cost estimate for hospitalized mild head injured patients at slightly over $900 million annually (Kraus and Nourjah 1989). Added to this figure is the cost of future medical consultations. future lost earnings and treatment costs. It has been estimated that 53% of whiplash patients take more than four weeks to recover. One year after the event.
2.9% remained unable to return to work. Given the variability in time frame for recovery.
these costs can be projected from weeks to years in any individual case. Since the peak incidence rate of whiplash injury occurs in the 20-54 year old age range (Spitzer et al.
1995), it predominantly affects a group of working people for whom lost wages can become a very costly factor in compensation.
Statistics cited from New York University suggest that the rate of post-concussion symptoms remains at approximately 10% at the end of a year. About 11% of people
10
employed before their injury are out of work at one year follow-up. Kay. Newman.
Cavallo. Ezrachi and Resnick ( 1992) in using a conservative estimate of 5% of patients with residual dysfunction following mild head injury. estimated 67,000 people are rendered dysfunctional by whiplash on an annual basis. Tease II ( 1993) stated that less than 10% of whiplash injured patients develop chronic ongoing pain. However. they estimated 40-70% of patients retain some degree of intermittent discomfort or ·•nuisance ··
symptoms which fluctuate from being distracting to occasionally intolerable. Given that at six months post-injury the person·s condition is considered chronic and prognosis for further recovery is guarded (Teasell 1993 ). these types of injuries are cumulative in the population (Kay 1992).
According to some accounts. neuropsychological investigation can be used in the absence of other supporting medical documentation to detect subtle changes in cognitive functions following such injuries (Gentilini, Nichelli and Schoenhuber 1989: Stuss eta/.
1985; Shapiro and Roth 1993; Anderson 1995). Neuropsychological findings can also be used to make recommendations regarding eventual return to employment or supported employment. These issues, which are becoming increasingly important from a medical-
legal perspective, have also affected personal injury claims in Ne\\foundland. Claims incorporating neuropsychological evidence incur increased costs through such
consultations. Higher compensation awards are typically offered when allegations of mild brain damage following whiplash is suggested (Taylor eta/. 1996).
There is an ongoing need to investigate the contribution of neuropsychological and psychological factors in the etiology, maintenance and perpetuation of symptoms associated with whiplash.
1.4 Post Concussion Symptoms 1.4.1 Physical Sequelae
1 1
Chronic. recurrent post-traumatic headaches. the most commonly reported physical complaint following minor head trauma can have a major disruptive effect for prolonged periods in individuals who have otherwise recovered (Bennett 1988). The economic impact of chronic headaches is significant in prevention of return to work. The
incidence of cervico-genic headaches in victims of cervical whiplash ranges from 50 to 87 % in the acute phase to 14 to 61 % in later stages (Radonov er a/. 1992). Although the pathogenesis of these headaches remains imprecise, they are usually unilateral. localised to the occipitocervical region. and can last for hours. They may be associated 'hith phono or photophobia, nausea. vomiting, irritability, vertigo, blurred vision. tearing and
conjunctival redness as well as hypoesthesia in the posterior region of the scalp (Spitzer et a/. 1995).
Irritation of the dura mater or the dural sac has been correlated with paravertebral spasm along multiple levels of the cervical spine with severe limitation of movement of the herniated disc. Sudden increase in pressure such as that elicited by coughing or effort may then trigger severe cervical pain. This has been proposed as the mechanism by which
12 a Cl to C3 injury results in pain in the suboccipital and temporal regions as well as in the periauricular region (Spitzer et a/. 1995).
For years patients who complained of head pain following mild head trauma were considered neurotics who either exaggerated or contrived their complaints for secondary gain. Though still incompletely understood it is becoming increasingly recognized that head pain is real and that early management is critical to prevent the establishment of chronic pain patterns (Larkin 1992}.
Other primary physical complaints associated with both the post-concussion syndrome as well as whiplash injury involves visual and acoustic hyperaesthesia (Bohnen. Twijnstra. Wijnen and Jolles 1992; Bagby 1992), as well as dizziness.
insomnia. fatigue and reduced tolerance to alcohol (Anderson 1995~ Davidoff et al.
1988).
The multiplicity of symptoms associated with the postconcussion syndrome has lead to difficulty in conceptualization and quantification of complaints (Levin. High.
Goethe. Sisson, Overall et a/ 1987). This is worsened by the interaction of the various symptoms involved. It is particularly apparent in patients who suffer pain over a
prolonged period of time. Kewman, Vaishampayan, Zald and Han (1991) established that cognitive impairments in memory and attention can exist in patients who suffer
musculoskeletal pain. Shapiro, T easell and Steenhuis ( 1993) cite Kewman' s research to support the view that cognitive complaints in whiplash patients is attributable to pain and does not reflect mild traumatic brain injury. However, Kewman and colleagues
13 themselves speculated undiagnosed organic brain dysfunction as well as low education level to be two contributing, confounding variables to their finding of cognitive
impairment in pain patients. They also suggested that these deficits, in combination with other factors including psychological distress to pain. adversely influenced cognitive status. Shapiro et a/. ( 1993) contend that most clinicians who work with chronic pain patients have observed that complaints of cognitive difficulty. particularly in memory and concentration, are quite prevalent.
Although the attribution of cognitive deficits in whiplash patients to mild brain injury has been advanced by some researchers. others contend that cognitive complaints are prevalent in chronic pain patients (Shapiro. Tease II and Steenhuis 1993 ). It has been suggested that people who suffer pain are distracted by sensory pain input which
interferes with cognitive functions such as memory. Although the possibility that chronic pain, in association with emotional disturbance. can have a negative impact on cognitive status cannot be denied, few empirical studies exist formally assessing
neuropsychological functions in pain patients. The studies that are available fail to compare results to clinically meaningful norms or standards (Kewman et al. 1991 ).
Two studies that did assess the relationship between cognitive deficits in pain patients relied on brief screening tools or few tests which limited interpretation of results (Kewman et ~/. 1991; Schwartz eta/. 1987). In Kewman's study, although 32% of the
musculoskeletal pain patients were impaired on the cognitive screening tool they utilized, the correlation between pain and cognitive impairment was reduced to insignificant when
14 psychological distress was accounted for. The authors suggest that although cognitive dysfunction is frequent in chronic pain patients, chi square analysis did not support a statistically significant correlation between these two factors. They recommend use of a more thorough comprehensive neuropsychological batt~ry. including more standardized measures of emotional distress, to more clearly define the relationship of cognitive compromise in pain patients (Kewman et a/. 1991 ).
Consistent findings were reported by Schwartz eta/. ( 1987) who compared cognitive performance in chronic pain patients with and without a history of head /neck injury. Measures used in their study to assess cognitive functions included the Trail Making Test (TMT). the Paced Auditory Serial Addition Test (PASAT). as well as a measure of verbal fluency. No mean differences were found between the groups on any of these tests. However cognitive impainnent ratings, based on the pattern of performance between the three tests. were highly significant when education was accounted for. The neck/head injured group was clearly more cognitively compromised compared with a predominantly low back pain population. Sixty-eight percent of the patients with a history of traumatic head or neck injury were impaired compared with only twenty-six percent of patients with chronic pain syndromes.
The relationship between pain severity and emotional response to it warrants further discussion. Kleinke ( 1991) hypothesised the interaction between chronic pain and depression may be mediated by such factors as appraisals of life interference due to physical discomfon as well as by perceived control of pain. It has been shown that
15 convictions of no control and helplessness are more highly correlated with L'1e perception of pain and disability than actual disease-related variables (Flor, Birbaumer and Turk
1990).
Closely related to perceived control is an individual's sense of self-efficacy. This refers to the conviction that one can successfully contend with a given situation and that situational demands will not exceed the ability to cope with them (Dolce 1987). Self- efficacy appears to play a significant role in the understanding of chronic pain. The higher the perceived sense of control. the lower the level of emotional arousal in stressful
situations. all of which have been correlated with changes in heart rate. blood pressure and serum catecholamine levels (Dolce 1987).
Active coping strategies. wherein patients take responsibility for their own pain management. have been associated ~ith lower levels of subjective reports of pain severity. reduced depression and less functional disability (Turner and Clancy 1986~
Jensen. Turner. Romano and Karoly 1991 ). In contrast to active strategies. passive
strategies such as reliance on the medical system or medication use, have been associated with increased pain severity, depression and functional disability. Pain, which occurs during activity may precipitate anxiety-related sympathetic activation with resultant increased muscle tension. Long periods of immobility will lead to muscular atrophy as well as a reduction in the ability of the muscles to restore and maintain stability (Fior et al. 1990). Pain patients often restrict their general activity level, including isolated body movements in the affected region. for fear of pain. This results in increased muscle
16
tension with no stress release mechanism so that muscles remain constricted resulting in heightened physical discomfort.
Depressed chronic pain patients have been consistently found to be less active than non~depressed controls (Haythornwaite. Sieber and Kerns 1992). Reduced activity for fear of pain has a direct effect on endogenous opiate release which may contribute to a maintenance or perpetuation of both physical discomfort and depression. A two to
fivefold increase in plasma concentrations of endorphins have been reported following such physical activity as running or S\.\imming (Daniel. Martin and Carter 1992). Activity may therefore play a potentially powerful therapeutic role in chronic pain management.
There is strong support for the proposal that physical activity induces endorphin~mediated
mood changes tending away from tension. anger. fatigue and depression. The analgesic.
behavioural and cardiovascular effects of exercise. mediated by endorphinergic mechanisms. favours a greater sense ofwell~being (Thoren eta/. 1990).
Empirical research measuring cognitive functions is sparse in patients suffering mild head and neck injury and virtually nonexistent in other chronic pain populations. It is therefore impossible to determine the relationship or etiological significance between cognitive deficits and pain in whiplash patients given limited research in this area.
1.4.2 Cognitive Sequelae
Together with physical complaints the incidence of cognitive deficits in patients suffering post-concussion symptoms is high. Schwartz et al. (1987) suggested that most of these patients focus predominantly on their pain and themselves attribute emotional,
behavioural and cognitive sequelae to secondary effects of pain. Despite this it has been speculated that vocational and social disruption may be a direct result of organicaily based cognitive deficits.
17
Stuss era/. ( 1983) suggested that mental deficits may persist in mild head injured patients even when the patient is otherwise considered to have made a good recovery.
They characterized residual deficits. primarily in divided attention. as a "limitation of the damaged brain in information processing capacity. either in terms of speed of processing or in terms of the amount of information that can be handled simultaneously" ( Stuss er a/.
1985). Other cognitive deficits experienced involved memory processes especially following a timed delay.
In a later study various parameters of attention vulnerable to the detrimental effects of head injury, regardless of severity, including those deficits experienced by concussed patients were further clarified (Stuss. Stethem, Hugenholtz, Picton. Pivik and Richard 1989). They maintained that such patients exhibit a deficit in complex attentional functions including divided attention. This they defined as the slowed conscious control of information processing coupled with au inability to contend with multiple pieces of information rapidly and easily. Impaired focussed and sustained attention was also apparent and limited the patients' ability to meet task demands. This resulted in
inconsistency in maintaining an optimal level of performance over time. Although not well investigated. the pathophysiology underlying these deficits has been postulated to
reflect a disruption in frontal-limbic-reticular activating system-brainstem control of anentional processes (Stuss eta!. 1985).
18
Without positive results using neuroimaging techniques documenting that concussion or mild traumatic brain injury has occurred, the value and sensitivity of neuropsychological evaluation has become recognized as providing clinical or functional evidence of organic brain dysfunction through disruption of cognitive functions
(Guilmette and Matazow 1992). However the subtle nature of residual
neuropsychological deficits necessitates that assessment procedures be sensitive enough to detect them. The need for psychometric testing within the context of a
multidisciplinary assessment and treatment approach for whiplash patients was more recently advocated by a Quebec task force studying whiplash associated disorders (WAD) (Spitzer eta/. 1995). Positive neuropsychological findings incorporated into research and clinical protocols can provide meaningful information on altered cognitive status. It can therefore help to determine the severity of the consequences of the injury. Results can also be used to facilitate return to previous vocational and lifestyle pursuits.
1.4.3 Emotional Sequelae
Affective consequences of post-concussion syndrome are common and include emotional lability and disinhibition (Davidoff eta/. 1988) as well as anxiety, irritability and depression (Levine 1988; Anderson 1995). Some feel that the evolution of these symptoms is a reaction to physical and cognitive effects of the injury. O'Hara, ( 1988) suggested such factors as lack of information to the patient to explain symptoms;
overlooked evidence of minor head trauma; or unsuccessful. premature return to work resulting in a failure experience and reduced self-esteem all contribute to
psychopathology. Such emotional reactions typically involve anxiety, irritability and depression.
19
Schoenhuber and Gentilini ( 1988) prospectively studied a group of mild head injured patients for neuropsychiatric complications. They found 77% of the patients studied showed an increased susceptibility to depression but they found no evidence of elevated state or trait anxiety using the Spielberger index (STAI). They attributed this
latter finding to inadequate sensitivity in the STAI to differentiate the two aspects of anxiety. They strongly recommend screening for depression in all patients suffering mild traumatic brain injury given its high incidence.
The lack of correspondence between subjective complaints and severity of head injury and the persistence of symptoms. together with these emotional factors. has been used to support the contention that post concussion symptoms are primarily of
psychological or motivational etiology. Indeed some clinicians conceive of post
concussion symptoms solely as a manifestation of a post-traumatic stress disorder (PTSD) (Davidoff eta/. 1988). However essential to the diagnosis of post-traumatic stress
disorder is the existence of intrusive ideas. as well as feelings or dreams about the trauma.
This is characterized by the persistent re-experiencing of the traumatic event (DSM IV 1994). These symptoms are not typically present in mild head injured patients (Binder 1986). Spitzer eta/. (1995) corroborate that PTSD, which typically occurs following
20 exposure to an unusually high-risk traumatic event causing temporary psychological destabilisation, does not hold true for whiplash patients. Orsillo and McCaffrey (1992) point out that symptoms in patients who experience even a brief period of post-traumatic amnesia (PTA) such as that which occurs following mild traumatic brain injury are more likely attributable to post-concussion symptoms. since the amnesia would preclude vivid recollection of the traumatic event critical to the diagnosis of PTSD. This argues against the anxiety theory accounting for all ongoing complaints following whiplash. However the importance of differential diagnosis between post-concussion symptoms and post- traumatic stress disorder given the considerable degree of overlap between somatic.
cognitive and affective symptoms should not be minimized.
Despite the ubiquity of emotional disturbance in patients suffering post
concussion symptoms and the attribution by proponents of the organic school of thought of cognitive deficits to structural brain damage, the pathogenesis of emotional
consequences remains almost exclusively attributed to psychological factors which develop secondary to the actual physical injury. This attribution may be premature given the association of personality change following significant head injury (Prigatano 1992) to structural brain lesions (Mattson and Levin 1990; Stuss, Gow and Hetherington 1992).
Speed (1993) further contends that there is considerable evidence to support the belief that mood changes following cervical strain or whiplash not only play a permanent role in the continuation of post-traumatic symptoms, but are directly related to the site of brain injury.
11
There is considerable overlap in emotional sequelae associated with post
concussion syndrome with brain damage of various other etiologies including head injury.
stroke, multiple sclerosis, or epilepsy (Roberts, Gorman, Lee, Hines. Richardson. Riggle
1992~ and Varney, Hines, Bailey and Roberts 1992). Commonly reported emotional concomitants of brain damage involve irritability, agitation. anger. abrupt episodic dyscontrol. emotional lability, anxiety, aspontaneity, reduced initiative, easy fatigue and depression. (Prigatano 1992). These symptoms have typically been associated with
fronto-temporal-limbic structures all of which are thought to modulate emotions. It seems not inconceivable therefore that emotional concomitants associated with post-concussion syndrome may be at least partially related to the site of cerebral damage and not solely reactionary to cognitive and physical change.
Derryberry eta/. ( 1992) caution against analysing one functional system or brain structure in detail or of hypothesizing that a deficit in a specific region can explain a clinical disorder given the "formidably complex" interdependence of the proposed levels of processing involved in emotional representation. Nevertheless, knowledge on neural substrates of emotions continues to advance. The evolutionary circuitry underlying emotions is considered to extend from the brainstem to the limbic system and from paralimbic regions to cortical structures (Derryberry and Tucker 1992). The network represents a hierarchal distribution of neural systems with an integration of information from the multiple levels of input involved. Emotional expression is commonly ascribed to the limbic system primarily because of its involvement in somatic and autonomic activity
22
(Orsillo and McCaffrey 1992). Although definitive statements cannot be made on neural mediation of affective symptoms, some evidence exists which may be useful. when supplemented with cognitive and physical information. in further elucidating the etiology of post concussion symptoms following hyperextension injury to the neck.
Few studies have investigated the possible neurological substrates of generalized anxiety disorder (GAD). In view of the paucity of studies. a single unifying perspective on the neuropsychology of anxiety has not been postulated. However it has been
hypothesized that patients with GAD experience a diminution of attentional capacity to external stimuli representing an information processing deficit. Further research in this area would contribute to a better understanding of lJI'lderlying neural substrates and the possible mechanism of action of post concussion symptoms. This is especially
noteworthy in view of the overlap of symptoms including impaired efficiency of information processing coupled with increased anxiety common to both anxiety and concussed patients.
In reviewing electrophysiological and neuroimaging results, Orsillo and McCaffrey ( 1992) found the consistent emergence of involvement of temporal lobe regions in the mediation of anxiety. The authors recommend that further
electrophysiological and brain-imaging assessment should be augmented by
neuropsychological assessment of memory processes to confirm the presence or absence of temporal lobe dysfunction in anxiety-disordered patients. They speculate that anxiety resulting from CNS damage may result from focal neurological disruption or may present
as an anxiety disorder according to DSM IV classification. Thus, similar or adjacent
.,
..._
_,neural pathways may underlie both cognitive deficits and affective dysfunction. Damage to regions involving brainstem and temporal lobe structures have been postulated to mediate both anxiety and PCS. This consistency supports the contention that some degree of affective dysfunction associated with post concussion syndrome may be structurally based.
Patients with whiplash injury have been shown to be more depressed and anxious than healthy controls (Lee et a/. 1993 ). It has also been shown that depression and high pain ratings were greater in patients with a longer history of pain (Lee et ai. 1993 ). These tindings have led to the suggestion that psychological disturbances are a secondary reaction associated with pain in whiplash patients and are not a primary feature of the diagnosis. Further, the longer the disruption to normal routines. the greater the likelihood of developing psychological reactions. It has been recognised that the presence of an.xio- depressive factors may influence the perception of a patient following whiplash injury and thereby perpetuate the emotional response to pain. This. in turn can exacerbate the painful experience itself (Spitzer eta/. 1995).
The presence of cognitive deficits due to cerebral dysfunction in patients with a history of head or neck injury and who experience pain can cause and in tum be amplified by reactive psycho-social distress (Schwartz et a!. 1987). Further. the stress associated with cognitive compromise may precipitate the development of a feedback loop causing increased muscle tension which can aggravate physical discomfort generated by muscular
24
skeletal problems. Increased muscle tension, also critical to the diagnosis of anxiety may be erroneously attributed to psychological distress without due regard for etiological factors which may have contributed to its development.
Psychological sequelae including depression and anxiety. commonly reponed in PCS patients following both whiplash and head injury. can have a potentially adverse effect on long-term outcome. That incidence rates of depression associated with traumatic brain injury vary greatly with ranges as wide as 10 to 77 percent (Rosenthal et a/. 1998) recognises the impact in terms of the number of patients suffering psychological distress.
Rosenthal et a/. ( 1998) attributed some of the variability in these depression ratings to lack of control for severity of head injury in the populations studied as well as to different methods used to diagnose the severity of the depression. Before lingering deficits
associated with PCS following either mild traumatic brain injury or whiplash are
attributed to brain damage. the contribution of these factors, which can have a deleterious effect on cognitive functions. should be considered. Shapiro ( 1993) recommends that decrements in cognitive status should be greater than expected as a consequence of co- existing affective symptoms or pain.
Historically, depression and anxiety following head injury was thought to reflect a psychological reaction to the injury. Merskey (1993) suggested that concentration
difficulties following mild traumatic brain injury may be due to the effects of depression.
Fox, Lees-Haley, Earnest and Dolezal-Wood (1995) point out that many complaints associated with PCS are common to a variety of psychological and medical conditions.
They suggest that given the considerable degree of overlap between psychological
..,- _,
symptoms associated with depression and anxiety and those experienced by patients with other neurological disorders such as forgetfulness and reduced concentration. it seems more logical to attribute cognitive deficits to a psychological reaction to the injury. In addition. it has been suggested that the development of psychological disturbance following acceleration injury is fostered by the medical system in feedback given to patients in the acute phase of illness. Early after injury, patients are often told their symptoms should resolve in three to six months. This message becomes counter-
therapeutic for the select group of patients who do not recover as anticipated within this time-frame (Mersky 1993). When patients continue to have lingering symptoms. they begin to feel there is some reason for their lack of recovery and that they may be
somehow to blame for not following recommendations. These concerns can precipitate psychological distress.
Neuropsychological deficits in clinically depressed patients typically cluster around three major areas of impairment. These include slowed psychomotor speed~
attention and motivational functions including difficulty perfonning tasks requiring sustained effort and concentration; and learning and memory (Sweet and Westergaard
1997). Learning and memory deficits have been further characterised and include impaired intentional memory; difficulty learning new and unfamiliar types of associations; as well as difficulty with free recall. In contrast, incidental recall and
26
recognition of information tends to be better preserved in depressed patients (Sweet and Westergaard 1997).
Findings of memory impairment in depressed patients, however, are certainly not conclusive as a number of studies have failed to find memory problems in clinically depressed patients (Newman and Sweet 1992). This may be attributed to the degree of depressive symptomatology present since some studies have found a correlation between severity of depression and neuropsychological test perfonnance. Typically severely depressed psychiatric in-patients perform more poorly than mildly to moderately depressed out-patients (Newman and Sweet 1992). Clearly the impact on
neuropsychological test performance in patients with a primary diagnosis of depression is not well understood and can lead to confusion when interpreting cognitive test results.
Future research should attempt to more clearly delineate the influence of reactive depression as well as feelings of dysphoria in both neurological and pain patients on neuropsychological findings to discern the etiology of cognitive compromise experienced.
As with depression, the impact of anxiety on neuropsychological test performance is often far from clear. It has been accepted that patients who are highly anxious in
general, as measured by high trait anxiety, are compromised on cognitive testing. Anxiety reduces the amount of available central executive capacity which, when directed to such activities as worry, leaves less capacity to focus attention on other cognitive processes (Shapiro et al. 1993). However in their review, Orsillo and McCaffrey ( 1992) suggest that anxiety does not significantly affect test performance, specifically in PTSD patients who
27
are clearly not severely compromised on neuropsychological testing compared to nonnative data. These authors also emphasize that although approximately 25 % of traumatic brain injury survivors. regardless of severity. suffer from increased anxiety or tension. only 10 % display a level of anxiety or depression considered clinically
significant. The distinction between the presence of anxiety symptoms that do not meet DSM-IV diagnostic criteria versus patients who do meet these criteria is. therefore critical (Orsillo and McCaffrey 1992).
Cognitively. similar to depression. new learning potential as well as concentration deficits have been associated with anxiety. In a review of lingering polysymptomatic complaints of mild traumatic brain injury. Putnam eta/. (1996) emphasize that state anxiety has been associated with cognitive impairment affecting working memory capacity. They therefore attribute lingering deficits experienced following mild brain damage to secondary changes associated with anxiety.
More recently, however, neurological techniques have confirmed neuroanatomic and neurochemical correlates of both depression and anxiety following brain injury which has helped to dispel the attribution of psychological disturbance in PCS solely to
secondary reaction to the injury. In his review, Rosenthal eta/. ( 1998) cites evidence that head injured patients with major depression showed lesions of the left dorso-lateral
frontal region and/or had lesions in the left basal ganglia. In fact they suggest that damage to the left basal ganglia may be critical to the development of depression.
28 Research investigating neurochemical correlates of depression have focussed on the biogenic amine system given its widespread distribution throughout the brain
(Rosenthal et al. 1998). Specifically, noradrenergic and serotonergic projections from the brainstem enter the cortex via the frontal pole. Collateral projections are then sent
throughout the neocortex. Given the propensity for damage to the frontal pole following acceleration injuries, it has been suggested that even a small lesion in this area could cause potential widespread disruption to cortical aminergic function. Despite these observations. Rosenthal et a/. ( 1998) asserts that knowledge on the neurobiological correlates of depression following brain injury is limited and therefore few conclusions can be drawn.
As with depression. neuroanatomical theories have been advanced to account for an.xiety-related symptoms which are most apparent in patients suffering chronic panic attacks. It has been proposed that a hierarchial progression of abnonnal brainstem function may explain autonomic symptomatology typical of anxiety. That is.
overactivation of specific brainstem nuclei involved in the control of respiration (nucleus solitarius). heart rate (nucleus ambiguus), bronchial constriction (nucleus ambiguus) and balance (vestibular nucleus) may occur. This activation, followed by overactivation of midbrain limbic structures including posterior hypothalamic nuclei, mesial temporal lobe, amygdala, hippocampus and orbital frontal lobes ( Orsillo and McCaffrey 1992), may contribute affective coloration and thereby the maintenance of anxiety symptoms.
29 Rosenthal et a/. ( 1 998) caution that dichotomizing depression in terms of primary and secondary disorders may be ·•grossly oversimplified"' since both forms of depression can occur concurrently. They propose that depression which occurs in the acute phase of head injury may be subserved by neurophysiological processes associated with the injury.
In contrast. late onset depression is more likely attributable to psychological factors.
Anxiety in patients suffering CNS trauma may also be due to focal neurological
disruption. may reflect subclinical levels. or may present as a DSM-IV disorder (Orsillo and McCaffrey 1992). Therefore anxiety may also reflect actual structural damage.
psychological response to trauma and residual cognitive and physical effects thereof. or a combination of both.
In addition to emotional changes associated with post concussion syndrome following whiplash or head injury. it has been argued that personality variables of long- standing origin influence whether or not patients suffer lingering symptoms. In their review article, Putnam er a/. ( 1996) emphasise the existence of a common personality type in traumatic brain injured patients characterised by a negativistic pattern with passive-aggressive traits as measured by the Millon Behavioral Health Inventory. These authors cite several papers in which it has been argued that neuroticism is a stable,
pervasive personality characteristic which is highly associated with self·report of physical symptoms. Youngjohn et al. ( 1995) also believe that personality traits influence the persistence of post concussion symptoms. In their study of 55 patients suffering ongoing complaints ofPCS following mild traumatic brain injury, elevations were apparent on the
30 somatisation index of the MMPI-2. They use this finding to support the hypothesis that persisting symptoms of PCS are likely functional in many patients and therefore not of organic etiology (Youngjohn et a/. 1995). The idea that premorbid characterological factors contribute to the maintenance ofPCS has not. however. been universally accepted (Robertson, Rath. Fournet. Zelhart and Estes 1994~ Gimse, Bjorgen. Tjell. Tyssedal and Bo 1997). Putnam et al. ( 1996) do acknowledge that the role of personality variables has not been adequately addressed in clinical neuropsychological studies.
1.4.4 Symptom Interaction
One of the few attempts to examine the relationship between physical complaints including head and neck pain and cognitive dysfunction in whiplash patients was
undertaken by a group of Swiss researchers (Radonov et al. 1992; 1993 ). They suggested that whiplash patients as a whole could be subdivided into two groups based on level of cervical injury. Patients who suffered injury to the upper spine complained of fatigue.
dizziness. reduced concentration. and disturbed adaptation to light intensity. In addition to slowed rate of information processing, these patients exhibited impaired divided
attention. These symptoms were classified as a ''cervicoencephalic syndrome" (CES).
Patients with lower cervical spine injury (LCSS) suffered predominantly cervical and cervicobrachial pain. They experienced no loss of consciousness at the time of trauma.
Although cognitive testing using the Paced Auditory Serial Addition Test (PASAT) revealed impaired divided attention in patients suffering CES, this was not present in the
31 LCSS group. As with CES patients, LCSS patients were impaired with respect to speed of infonnation processing.
Each group therefore demonstrated a unique symptom-complex involving
cognitive deficits. Based on these fmdings, the authors recommended the classification of whiplash patients into more precise subgroups be vigorously tested using objective
clinical data. To date. only limited positive findings using conventional radiographic diagnostic procedures are available to support this view (Gimse eta/. 1997). In Radonov's
1992 study. only 20 ofthe 45 whiplash patients studied showed observable lesions of the cervical spine. Of these. 5 had damage in the upper cervical region while 15 sustained injury in the mid to lower cervical region. Fifty-six percent of the whiplash patients showed ·no objective evidence of pathology· (NOEP) on standard radiological or medical investigation.
In an attempt to differentiate the effects of pain on cognitive status. Schwartz er a/. ( 1987) studied a group of chronic pain patients with and without a history of head or neck trauma sustained in rear-end motor vehicle collisions. They found a higher incidence of cognitive disturbance characterized by impaired sustained attention and reduced rapid problem-solving ability in the fanner group of patients. They emphasized several key points including the finding that the incidence and duration of subtle cognitive deficits in this population is greater than previously recognized. In addition cognitive deficits combined with pain results in more significant disruption in life functioning than would result from pain alone. Finally although deficits were subtle, they generated enormous
